Effects of 3,3′,4,4′,5,5′‐hexachlorobiphenyl on cytochrome P4501A and estrogen‐induced vitellogenesis in rainbow trout (Oncorhynchus mykiss)

Abstract

AbstractEstrogen‐regulated synthesis of vitellogenin (Vg), a yolk‐protein equired for reproduction, was monitored to explore the potential antiestrogenic effects of the coplanar polychlorinated biphenyl (PCB), 3,3′,4,4′,5,5′‐hexachlorobiphenyl (3,4,5‐HCB), in juvenile rainbow trout (Oncorhynchus mykiss). The effects of 17β‐estradiol on 3,4,5‐HCB induction of cytochrome P4501A (CYP1A) were also examined. Trout were injected with 3,4,5‐HCB (0.25, 2.5, 25, 50, or 100 mg/kg) or a vehicle control, and after 10 weeks, they were sampled or injected with 17β‐estradiol (0.1 mg/kg). Markers of vitellogenesis, such as liver somatic index, hepatic estrogen‐binding sites, and plasma Vg concentrations, in 17β‐estradiol‐treated fish were not affected by 3,4,5‐HCB. Maximal induction of CYP1A protein and mRNA occurred at doses above 2.5 mg/kg, and 17β‐estradiol reduced CYP1A protein content at a single dose (0.25 μg 3,4,5‐HCB/kg). Ethoxyresorufin‐O‐deethylase (EROD) activity was induced by 3,4,5‐HCB doses of between 0.25 and 2.5 mg/kg, but induction was reduced at higher doses, indicating that 3,4,5‐HCB suppressed CYP1A catalytic activity. In 3,4,5‐HCB/17β‐estradiol—treated fish, plasma estradiol was significantly reduced at 100 mg 3,4,5‐HCB/kg, but the depression was not associated with CYP1A induction or with other antiestrogenic effects. Although CYP1A was induced, 3,4,5‐ HCB did not interfere with vitellogenesis, which suggests that the PCB congener is not a potent antiestrogen in rainbow trout.